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Journal articles on the topic 'Neural progenitor'

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Published: 4 June 2021
Last updated: 22 February 2023

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1

Easterday, Mathew C., Joseph D. Dougherty, Robert L. Jackson, Jing Ou, Ichiro Nakano, Andres A. Paucar, Babak Roobini, et al. "Neural progenitor genes." Developmental Biology 264, no. 2 (December 2003): 309–22. http://dx.doi.org/10.1016/j.ydbio.2003.09.003.

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2

Allen, Nicholas D. "Temporal and epigenetic regulation of neurodevelopmental plasticity." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1489 (February 20, 2007): 23–38. http://dx.doi.org/10.1098/rstb.2006.2010.

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The anticipated therapeutic uses of neural stem cells depend on their ability to retain a certain level of developmental plasticity. In particular, cells must respond to developmental manipulations designed to specify precise neural fates. Studies in vivo and in vitro have shown that the developmental potential of neural progenitor cells changes and becomes progressively restricted with time. For in vitro cultured neural progenitors, it is those derived from embryonic stem cells that exhibit the greatest developmental potential. It is clear that both extrinsic and intrinsic mechanisms determine the developmental potential of neural progenitors and that epigenetic, or chromatin structural, changes regulate and coordinate hierarchical changes in fate-determining gene expression. Here, we review the temporal changes in developmental plasticity of neural progenitor cells and discuss the epigenetic mechanisms that underpin these changes. We propose that understanding the processes of epigenetic programming within the neural lineage is likely to lead to the development of more rationale strategies for cell reprogramming that may be used to expand the developmental potential of otherwise restricted progenitor populations.
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3

Shih, Hung-Yu, Chia-Wei Chang, Yi-Chieh Chen, and Yi-Chuan Cheng. "Identification of the Time Period during Which BMP Signaling Regulates Proliferation of Neural Progenitor Cells in Zebrafish." International Journal of Molecular Sciences 24, no. 2 (January 15, 2023): 1733. http://dx.doi.org/10.3390/ijms24021733.

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Bone morphogenetic protein (BMP) signaling regulates neural induction, neuronal specification, and neuronal differentiation. However, the role of BMP signaling in neural progenitors remains unclear. This is because interruption of BMP signaling before or during neural induction causes severe effects on subsequent neural developmental processes. To examine the role of BMP signaling in the development of neural progenitors in zebrafish, we bypassed the effect of BMP signaling on neural induction and suppressed BMP signaling at different time points during gastrulation using a temporally controlled transgenic line carrying a dominant-negative form of Bmp receptor type 1aa and a chemical inhibitor of BMP signaling, DMH1. Inhibiting BMP signaling from 8 hpf could bypass BMP regulation on neural induction, induce the number of proliferating neural progenitors, and reduce the number of neuronal precursors. Inhibiting BMP signaling upregulates the expression of the Notch downstream gene hairy/E(spl)-related 2 (her2). Inhibiting Notch signaling or knocking down the Her2 function reduced neural progenitor proliferation, whereas inactivating BMP signaling in Notch-Her2 deficient background restored the number of proliferating neural progenitors. These results reveal the time window for the proliferation of neural progenitors during zebrafish development and a fine balance between BMP and Notch signaling in regulating the proliferation of neural progenitor cells.
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4

Lillien, Laura. "Neural progenitors and stem cells: mechanisms of progenitor heterogeneity." Current Opinion in Neurobiology 8, no. 1 (February 1998): 37–44. http://dx.doi.org/10.1016/s0959-4388(98)80006-8.

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5

Mitra, Siddhartha S., Abdullah H. Feroze, Sharareh Gholamin, Chase Richard, Rogelio Esparza, Michael Zhang, Tej D. Azad, et al. "Neural Placode Tissue Derived From Myelomeningocele Repair Serves as a Viable Source of Oligodendrocyte Progenitor Cells." Neurosurgery 77, no. 5 (July 29, 2015): 794–802. http://dx.doi.org/10.1227/neu.0000000000000918.

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Abstract BACKGROUND: The presence, characteristics, and potential clinical relevance of neural progenitor populations within the neural placodes of myelomeningocele patients remain to be studied. Neural stem cells are known to reside adjacent to ependyma-lined surfaces along the central nervous system axis. OBJECTIVE: Given such neuroanatomic correlation and regenerative capacity in fetal development, we assessed myelomeningocele-derived neural placode tissue as a potentially novel source of neural stem and progenitor cells. METHODS: Nonfunctional neural placode tissue was harvested from infants during the surgical repair of myelomeningocele and subsequently further analyzed by in vitro studies, flow cytometry, and immunofluorescence. To assess lineage potential, neural placode-derived neurospheres were subjected to differential media conditions. Through assessment of platelet-derived growth factor receptor α (PDGFRα) and CD15 cell marker expression, Sox2+Olig2+ putative oligodendrocyte progenitor cells were successfully isolated. RESULTS: PDGFRαhiCD15hi cell populations demonstrated the highest rate of self-renewal capacity and multipotency of cell progeny. Immunofluorescence of neural placode-derived neurospheres demonstrated preferential expression of the oligodendrocyte progenitor marker, CNPase, whereas differentiation to neurons and astrocytes was also noted, albeit to a limited degree. CONCLUSION: Neural placode tissue contains multipotent progenitors that are preferentially biased toward oligodendrocyte progenitor cell differentiation and presents a novel source of such cells for use in the treatment of a variety of pediatric and adult neurological disease, including spinal cord injury, multiple sclerosis, and metabolic leukoencephalopathies.
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6

Feng, Shiqing, Juan Xiao, Fabin Han, Lin Chen, Wenyong Gao, Gengsheng Mao, and Hongyun Huang. "Neurorestorative clinical application standards for the culture and quality control of neural progenitor/precursor cells (version 2017)." Journal of Neurorestoratology 1, no. 1 (2018): 32–36. http://dx.doi.org/10.2147/jn.s147917.

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In order to promote the clinical use of neural progenitor or precursor cells for treating neurological diseases and damage, we need to standardize culture procedures for these cells. The Chinese Association of Neurorestoratology put forward these standards for training operators, standardized use and management of materials and equipment, standardized isolation and culture for neural progenitor/precursor cells, and the standardized management in preservation, transport, and related safe operation procedures of the neural progenitors. These cultures and quality control standards also include the Good Manufacturing Practice environment, routine maintenance as well as the monitoring and reporting of the clinical-grade neural progenitor cells. The aim of these standards is to improve the therapeutic efficacy and minimize the possible side effects from lake of quality control.
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7

Hill, Justin, and John Cave. "Targeting the vasculature to improve neural progenitor transplant survival." Translational Neuroscience 6, no. 1 (January 1, 2015): 162–67. http://dx.doi.org/10.1515/tnsci-2015-0016.

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AbstractNeural progenitor transplantation is a promising therapeutic option for several neurological diseases and injuries. In nearly all human clinical trials and animal models that have tested this strategy, the low survival rate of progenitors after engraftment remains a significant challenge to overcome. Developing methods to improve the survival rate will reduce the number of cells required for transplant and will likely enhance functional improvements produced by the procedure. Here we briefly review the close relationship between the blood vasculature and neural progenitors in both the embryo and adult nervous system. We also discuss previous studies that have explored the role of the vasculature and hypoxic pre-conditioning in neural transplants. From these studies, we suggest that hypoxic pre-conditioning of a progenitor pool containing both neural and endothelial cells will improve engrafted transplanted neuronal survival rates.
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8

Sánchez-González, Rebeca, María Figueres-Oñate, Ana Cristina Ojalvo-Sanz, and Laura López-Mascaraque. "Cell Progeny in the Olfactory Bulb after Targeting Specific Progenitors with Different UbC-StarTrack Approaches." Genes 11, no. 3 (March 13, 2020): 305. http://dx.doi.org/10.3390/genes11030305.

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The large phenotypic variation in the olfactory bulb may be related to heterogeneity in the progenitor cells. Accordingly, the progeny of subventricular zone (SVZ) progenitor cells that are destined for the olfactory bulb is of particular interest, specifically as there are many facets of these progenitors and their molecular profiles remain unknown. Using modified StarTrack genetic tracing strategies, specific SVZ progenitor cells were targeted in E12 mice embryos, and the cell fate of these neural progenitors was determined in the adult olfactory bulb. This study defined the distribution and the phenotypic diversity of olfactory bulb interneurons from specific SVZ-progenitor cells, focusing on their spatial pallial origin, heterogeneity, and genetic profile.
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9

Alshawaf, Abdullah J., Ana Antonic, Efstratios Skafidas, Dominic Chi-Hung Ng, and Mirella Dottori. "WDR62 Regulates Early Neural and Glial Progenitor Specification of Human Pluripotent Stem Cells." Stem Cells International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/7848932.

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Mutations in WD40-repeat protein 62 (WDR62) are commonly associated with primary microcephaly and other developmental cortical malformations. We used human pluripotent stem cells (hPSC) to examine WDR62 function during human neural differentiation and model early stages of human corticogenesis. Neurospheres lacking WDR62 expression showed decreased expression of intermediate progenitor marker, TBR2, and also glial marker, S100β. In contrast, inhibition of c-Jun N-terminal kinase (JNK) signalling during hPSC neural differentiation induced upregulation of WDR62 with a corresponding increase in neural and glial progenitor markers, PAX6 and EAAT1, respectively. These findings may signify a role of WDR62 in specifying intermediate neural and glial progenitors during human pluripotent stem cell differentiation.
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10

Ruan, Xiangbin, Bowei Kang, Cai Qi, Wenhe Lin, Jingshu Wang, and Xiaochang Zhang. "Progenitor cell diversity in the developing mouse neocortex." Proceedings of the National Academy of Sciences 118, no. 10 (March 1, 2021): e2018866118. http://dx.doi.org/10.1073/pnas.2018866118.

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In the mammalian neocortex, projection neuron types are sequentially generated by the same pool of neural progenitors. How neuron type specification is related to developmental timing remains unclear. To determine whether temporal gene expression in neural progenitors correlates with neuron type specification, we performed single-cell RNA sequencing (scRNA-Seq) analysis of the developing mouse neocortex. We uncovered neuroepithelial cell enriched genes such as Hmga2 and Ccnd1 when compared to radial glial cells (RGCs). RGCs display dynamic gene expression over time; for instance, early RGCs express higher levels of Hes5, and late RGCs show higher expression of Pou3f2. Interestingly, intermediate progenitor cell marker gene Eomes coexpresses temporally with known neuronal identity genes at different developmental stages, though mostly in postmitotic cells. Our results delineate neural progenitor cell diversity in the developing mouse neocortex and support that neuronal identity genes are transcriptionally evident in Eomes-positive cells.
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11

Porat, Yael, Valentin Fulga, Danny Belkin, Svetlana Porozov, Yehudit Fisher, Michael Belkin, and Willam F. Silverman. "Adult Human Blood Leukocytes as an Efficient Source for Tissue-Committed Neural Progenitors." Blood 106, no. 11 (November 16, 2005): 1686. http://dx.doi.org/10.1182/blood.v106.11.1686.1686.

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Abstract In the last few years, significant progress has been made in the isolation and characterization of bone marrow stem cell populations and their potential to differentiate into a variety of cellular lineages. We hypothesized that peripheral blood can also be used as a source for precursor cells that can become committed progenitors for a variety of tissues. We report here the generation and characterization in vitro of neural progenitor cells from a newly discovered blood-derived multipotent cell population, named synergetic cell population (SCP). Human blood samples were obtained from the Israeli blood bank and SCP cells were purified based on cellular density. Neural progenitors were generated by culturing SCP cells in medium supplemented with autologous serum, followed by activation in a defined serum-free medium containing the specific differentiation-inducing factors F12, B27, bFGF, BDNF, and NGF. An average of 13.5x106 neural progenitor cells was generated from 450 ml blood. These cells developed irregular perikarya, from which filamentous extensions spread contacting neighboring cells and forming net-like structures. Immunostaining revealed that some of the cells express the early neuronal progenitor markers nestin and b-tubulin and Neu-N, a nuclear protein present in mature neurons. Other cells expressed glial-specific antigens, such as O4 (a marker of oligodendrocytes) and GFAP (a marker of astrocytes). Flow cytometry analysis showed that 44.4% and 34% of the cells were positive for nestin and b-tubulin, respectively. In addition to exhibiting phenotypic evidence of markers specific for the neural lineage, these progenitor cells also responded to the neurotransmitters glutamate and GABA, as detected by calcium influx through voltage-gated calcium channels, demonstrating functional differentiation. In this study we show that generation of neural progenitors from peripheral blood is feasible and efficient. Blood-derived angiogenic progenitors produced in our system are already safely and efficiently administrated to severe angina pectoris patients in a clinical trial we are conducting in Thailand (reported in a separate abstract by our group). The newly discovered source of these progenitors, the blood-derived multipotent population which we termed SCP, contains both hematopoietic stem cells as well as supportive cells that enable differentiation into various lineages. The therapeutic potential of these neural progenitors will be further characterized and evaluated in vivo using animal models.
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12

Osman, Ahmed M., Michelle J. Porritt, Michael Nilsson, and H. Georg Kuhn. "Long-Term Stimulation of Neural Progenitor Cell Migration After Cortical Ischemia in Mice." Stroke 42, no. 12 (December 2011): 3559–65. http://dx.doi.org/10.1161/strokeaha.111.627802.

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Background and Purpose— Cortical ischemia induces neural progenitor cell migration toward the injury site; however, whether these cells are capable of maintaining the migratory response for a longer period after injury remains uncertain. Methods— We analyzed progenitor migration up to 1 year after induction of photothrombotic stroke to the mouse neocortex. Migrating progenitors identified as doublecortin positive cells (DCX + ) were assessed using the immunohistochemistry and immunofluorescence. The thymidine analogues chlorodeoxyuridine and iododeoxyuridine were used to birth-date the progenitor cells. Results— In the striatum, we detected elevated numbers of DCX + cells up to 6 weeks postlesion. In the corpus callosum and the peri-infarct cortex (Ctx), DCX + cell numbers were increased up to 1 year. The orientation of the migrating progenitors was mostly aligned with the corpus callosum fiber tract at all time points; however, in the Ctx, they aligned parallel to the infarct border. The injured cortex continuously receives new progenitors up to 1 year after lesion. Cells born after lesion did not become mature neurons, although a portion of the migrating progenitors showed initial signs of differentiation into neurons. Conclusions— Neural progenitors might have a role in brain plasticity after cortical stroke, especially considering the prolonged window of migratory responses of up to 1 year after stroke lesion.
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13

Kendall, Stephen E., Chiara Battelli, Sarah Irwin, Jane G. Mitchell, Carlotta A. Glackin, and Joseph M. Verdi. "NRAGE Mediates p38 Activation and Neural Progenitor Apoptosis via the Bone Morphogenetic Protein Signaling Cascade." Molecular and Cellular Biology 25, no. 17 (September 1, 2005): 7711–24. http://dx.doi.org/10.1128/mcb.25.17.7711-7724.2005.

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ABSTRACT Understanding the molecular events that govern neural progenitor lineage commitment, mitotic arrest, and differentiation into functional progeny are germane to our understanding of neocortical development. Members of the family of bone morphogenetic proteins (BMPs) play pivotal roles in regulating neural differentiation and apoptosis during neurogenesis through combined actions involving Smad and TAK1 activation. We demonstrate that BMP signaling is required for the induction of apoptosis of neural progenitors and that NRAGE is a mandatory component of the signaling cascade. NRAGE possesses the ability to bind and function with the TAK1-TAB1-XIAP complex facilitating the activation of p38. Disruption of NRAGE or any other member of the noncanonical signaling cascaded is sufficient to block p38 activation and thus the proapoptotic signals generated through BMP exposure. The function of NRAGE is independent of Smad signaling, but the introduction of a dominant-negative Smad5 also rescues neural progenitor apoptosis, suggesting that both canonical and noncanonical pathways can converge and regulate BMP-mediated apoptosis. Collectively, these results establish NRAGE as an integral component in BMP signaling and clarify its role during neural progenitor development.
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14

Vukicevic, Vladimir, Janine Schmid, Andreas Hermann, Sven Lange, Nan Qin, Linda Gebauer, Kuei-Fang Chung, et al. "Differentiation of Chromaffin Progenitor Cells to Dopaminergic Neurons." Cell Transplantation 21, no. 11 (November 2012): 2471–86. http://dx.doi.org/10.3727/096368912x638874.

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The differentiation of dopamine-producing neurons from chromaffin progenitors might represent a new valuable source for replacement therapies in Parkinson's disease. However, characterization of their differentiation potential is an important prerequisite for efficient engraftment. Based on our previous studies on isolation and characterization of chromaffin progenitors from adult adrenals, this study investigates their potential to produce dopaminergic neurons and means to enhance their dopaminergic differentiation. Chromaffin progenitors grown in sphere culture showed an increased expression of nestin and Mash1, indicating an increase of the progenitor subset. Proneurogenic culture conditions induced the differentiation into neurons positive for neural markers β-III-tubulin, MAP2, and TH accompanied by a decrease of Mash1 and nestin. Furthermore, Notch2 expression decreased concomitantly with a downregulation of downstream effectors Hes1 and Hes5 responsible for self-renewal and proliferation maintenance of progenitor cells. Chromaffin progenitor-derived neurons secreted dopamine upon stimulation by potassium. Strikingly, treatment of differentiating cells with retinoic and ascorbic acid resulted in a twofold increase of dopamine secretion while norepinephrine and epinephrine were decreased. Initiation of dopamine synthesis and neural maturation is controlled by Pitx3 and Nurr1. Both Pitx3 and Nurr1 were identified in differentiating chromaffin progenitors. Along with the gained dopaminergic function, electrophysiology revealed features of mature neurons, such as sodium channels and the capability to fire multiple action potentials. In summary, this study elucidates the capacity of chromaffin progenitor cells to generate functional dopaminergic neurons, indicating their potential use in cell replacement therapies.
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15

Findlay, Quan, Kiryu K. Yap, Annette J. Bergner, Heather M. Young, and Lincon A. Stamp. "Enteric neural progenitors are more efficient than brain-derived progenitors at generating neurons in the colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 7 (October 1, 2014): G741—G748. http://dx.doi.org/10.1152/ajpgi.00225.2014.

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Gut motility disorders can result from an absent, damaged, or dysfunctional enteric nervous system (ENS). Cell therapy is an exciting prospect to treat these enteric neuropathies and restore gut motility. Previous studies have examined a variety of sources of stem/progenitor cells, but the ability of different sources of cells to generate enteric neurons has not been directly compared. It is important to identify the source of stem/progenitor cells that is best at colonizing the bowel and generating neurons following transplantation. The aim of this study was to compare the ability of central nervous system (CNS) progenitors and ENS progenitors to colonize the colon and differentiate into neurons. Genetically labeled CNS- and ENS-derived progenitors were cocultured with aneural explants of embryonic mouse colon for 1 or 2.5 wk to assess their migratory, proliferative, and differentiation capacities, and survival, in the embryonic gut environment. Both progenitor cell populations were transplanted in the postnatal colon of mice in vivo for 4 wk before they were analyzed for migration and differentiation using immunohistochemistry. ENS-derived progenitors migrated further than CNS-derived cells in both embryonic and postnatal gut environments. ENS-derived progenitors also gave rise to more neurons than their CNS-derived counterparts. Furthermore, neurons derived from ENS progenitors clustered together in ganglia, whereas CNS-derived neurons were mostly solitary. We conclude that, within the gut environment, ENS-derived progenitors show superior migration, proliferation, and neuronal differentiation compared with CNS progenitors.
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16

Goldman, Steve. "Glia as neural progenitor cells." Trends in Neurosciences 26, no. 11 (November 2003): 590–96. http://dx.doi.org/10.1016/j.tins.2003.09.011.

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17

Taverna, Elena, and Wieland B. Huttner. "Neural Progenitor Nuclei IN Motion." Neuron 67, no. 6 (September 2010): 906–14. http://dx.doi.org/10.1016/j.neuron.2010.08.027.

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18

ONIFER. "Potential of immortalized neural progenitor." Cell Transplantation 5, no. 5 (September 1996): 75. http://dx.doi.org/10.1016/0963-6897(96)82305-0.

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19

Sahu, Sanjeeb Kumar, Alina Fritz, Neha Tiwari, Zsuzsa Kovacs, Alireza Pouya, Verena Wüllner, Pablo Bora, et al. "TOX3 regulates neural progenitor identity." Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms 1859, no. 7 (July 2016): 833–40. http://dx.doi.org/10.1016/j.bbagrm.2016.04.005.

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20

Wang, Lei, Michael Chopp, Sara R. Gregg, Rui Lan Zhang, Hua Teng, Angela Jiang, Yifan Feng, and Zheng Gang Zhang. "Neural Progenitor Cells Treated with EPO Induce Angiogenesis through the Production of Vegf." Journal of Cerebral Blood Flow & Metabolism 28, no. 7 (April 16, 2008): 1361–68. http://dx.doi.org/10.1038/jcbfm.2008.32.

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Recombinant human erythropoietin (rhEPO) induces neurogenesis and angiogenesis. Using a coculture system of mouse brain endothelial cells (MBECs) and neural progenitor cells derived from the subventricular zone of adult mouse, we investigated the hypothesis that neural progenitor cells treated with rhEPO promote angiogenesis. Treatment of neural progenitor cells with rhEPO significantly increased their expression and secretion of vascular endothelial growth factor (VEGF) and activated phosphatidylinositol 3-kinase/Akt (PI3K/Akt) and extracellular signal-regulated kinase (ERK1/2). Selective inhibition of the Akt and ERK1/2 signaling pathways significantly attenuated the rhEPO-induced VEGF expression in neural progenitor cells. The supernatant harvested from neural progenitor cells treated with rhEPO significantly increased the capillary-like tube formation of MBECs. SU1498, a specific VEGF type-2 receptor (VEGFR2) antagonist, abolished the supernatant-enhanced angiogenesis. In addition, coculture of MBECs with neural progenitor cells treated with rhEPO substantially increased VEGFR2 mRNA and protein levels in MBECs. These in vitro results suggest that EPO enhances VEGF secretion in neural progenitor cells through activation of the PI3K/Akt and ERK1/2 signaling pathways and that neural progenitor cells treated with rhEPO upregulate VEGFR2 expression in cerebral endothelial cells, which along with VEGF secreted by neural progenitor cells promotes angiogenesis.
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21

Krieger, Teresa G., Carla M. Moran, Alberto Frangini, W. Edward Visser, Erik Schoenmakers, Francesco Muntoni, Chris A. Clark, et al. "Mutations in thyroid hormone receptor α1 cause premature neurogenesis and progenitor cell depletion in human cortical development." Proceedings of the National Academy of Sciences 116, no. 45 (October 18, 2019): 22754–63. http://dx.doi.org/10.1073/pnas.1908762116.

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Mutations in the thyroid hormone receptor α 1 gene (THRA) have recently been identified as a cause of intellectual deficit in humans. Patients present with structural abnormalities including microencephaly, reduced cerebellar volume and decreased axonal density. Here, we show that directed differentiation of THRA mutant patient-derived induced pluripotent stem cells to forebrain neural progenitors is markedly reduced, but mutant progenitor cells can generate deep and upper cortical layer neurons and form functional neuronal networks. Quantitative lineage tracing shows that THRA mutation-containing progenitor cells exit the cell cycle prematurely, resulting in reduced clonal output. Using a micropatterned chip assay, we find that spatial self-organization of mutation-containing progenitor cells in vitro is impaired, consistent with down-regulated expression of cell–cell adhesion genes. These results reveal that thyroid hormone receptor α1 is required for normal neural progenitor cell proliferation in human cerebral cortical development. They also exemplify quantitative approaches for studying neurodevelopmental disorders using patient-derived cells in vitro.
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Jolly, Lachlan A., Verdon Taylor, and Stephen A. Wood. "USP9X Enhances the Polarity and Self-Renewal of Embryonic Stem Cell-derived Neural Progenitors." Molecular Biology of the Cell 20, no. 7 (April 2009): 2015–29. http://dx.doi.org/10.1091/mbc.e08-06-0596.

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The substrate-specific deubiquitylating enzyme USP9X is a putative “stemness” gene expressed in many progenitor cell populations. To test its function in embryonic stem cell-derived neural progenitor/stem cells, we expressed USP9X from a Nestin promoter. Elevated USP9X levels resulted in two phenomena. First, it produced a dramatically altered cellular architecture wherein the majority (>80%) of neural progenitors was arranged into radial clusters. These progenitors expressed markers of radial glial cells and were highly polarized with adherens junction proteins (N-cadherin, β-catenin, and AF-6) and apical markers (Prominin1, atypical protein kinase C-ζ) as well as Notch, Numb, and USP9X itself, concentrated at the center. The cluster centers were also devoid of nuclei and so resembled the apical end-feet of radial progenitors in the neural tube. Second, USP9X overexpression caused a fivefold increase in the number of radial progenitors and neurons, in the absence of exogenous growth factors. 5-Bromo-2′-deoxyuridine labeling, as well as the examination of the brain lipid-binding protein:βIII-tubulin ratio, indicated that nestin-USP9X enhanced the self-renewal of radial progenitors but did not block their subsequent differentiation to neurons and astrocytes. nestin-USP9X radial progenitors reformed clusters after passage as single cells, whereas control cells did not, suggesting it aids the establishment of polarity. We propose that USP9X-induced polarization of these neural progenitors results in their radial arrangement, which provides an environment conducive for self-renewal.
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Tsupykov, O. "A protocol for isolation of fetal neural progenitor cells from mouse hippocampus." Cell and Organ Transplantology 2, no. 2 (November 30, 2014): 155–57. http://dx.doi.org/10.22494/cot.v2i2.32.

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Culture of neural stem/progenitor cells are widely used to study the characteristics of these cells under controlled conditions in vitro as well as to study the cellular and molecular mechanisms of CNS diseases and develop strategies for their treatment.This paper provides a detailed protocol to isolate of fetal (E17-18) neural progenitor cells (NPCs) of mouse hippocampus. The technique is based on the use of centrifugation of hippocampal cells suspension in Percoll density gradient to obtain purified NPCs fractions. The cells are cultured in serum-free medium in a monolayer, which creates conditions for more equitable access of FGF-2 to the cells. This method provides a homogeneous population of undifferentiated progenitors from fetal mouse hippocampus.
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Teng, Hua, Zheng Gang Zhang, Lei Wang, Rui Lan Zhang, Li Zhang, Dan Morris, Sara R. Gregg, et al. "Coupling of Angiogenesis and Neurogenesis in Cultured Endothelial Cells and Neural Progenitor Cells after Stroke." Journal of Cerebral Blood Flow & Metabolism 28, no. 4 (October 31, 2007): 764–71. http://dx.doi.org/10.1038/sj.jcbfm.9600573.

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Angiogenesis and neurogenesis are coupled processes. Using a coculture system, we tested the hypothesis that cerebral endothelial cells activated by ischemia enhance neural progenitor cell proliferation and differentiation, while neural progenitor cells isolated from the ischemic subventricular zone promote angiogenesis. Coculture of neural progenitor cells isolated from the subventricular zone of the adult normal rat with cerebral endothelial cells isolated from the stroke boundary substantially increased neural progenitor cell proliferation and neuronal differentiation and reduced astrocytic differentiation. Conditioned medium harvested from the stroke neural progenitor cells promoted capillary tube formation of normal cerebral endothelial cells. Blockage of vascular endothelial growth factor receptor 2 suppressed the effect of the endothelial cells activated by stroke on neurogenesis as well as the effect of the supernatant obtained from stroke neural progenitor cells on angiogenesis. These data suggest that angiogenesis couples to neurogenesis after stroke and vascular endothelial growth factor likely mediates this coupling.
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Desai, A. R., and S. K. McConnell. "Progressive restriction in fate potential by neural progenitors during cerebral cortical development." Development 127, no. 13 (July 1, 2000): 2863–72. http://dx.doi.org/10.1242/dev.127.13.2863.

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During early stages of cerebral cortical development, progenitor cells in the ventricular zone are multipotent, producing neurons of many layers over successive cell divisions. The laminar fate of their progeny depends on environmental cues to which the cells respond prior to mitosis. By the end of neurogenesis, however, progenitors are lineally committed to producing upper-layer neurons. Here we assess the laminar fate potential of progenitors at a middle stage of cortical development. The progenitors of layer 4 neurons were first transplanted into older brains in which layer 2/3 was being generated. The transplanted neurons adopted a laminar fate appropriate for the new environment (layer 2/3), revealing that layer 4 progenitors are multipotent. Mid-stage progenitors were then transplanted into a younger environment, in which layer 6 neurons were being generated. The transplanted neurons bypassed layer 6, revealing that layer 4 progenitors have a restricted fate potential and are incompetent to respond to environmental cues that trigger layer 6 production. Instead, the transplanted cells migrated to layer 4, the position typical of their origin, and also to layer 5, a position appropriate for neither the host nor the donor environment. Because layer 5 neurogenesis is complete by the stage that progenitors were removed for transplantation, restrictions in laminar fate potential must lag behind the final production of a cortical layer. These results suggest that a combination of intrinsic and environmental cues controls the competence of cortical progenitor cells to produce neurons of different layers.
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Ocwieja, K. E., T. K. Hughes, C. C. M. Baker, A. C. Stanton, J. M. Antonucci, A. L. Richards, A. Shalek, R. Jaenisch, and L. Gehrke. "#33: Single-cell RNA sequencing analysis of Zika virus infection in human stem cell-derived neuroprogenitor cells and cerebral organoids." Journal of the Pediatric Infectious Diseases Society 10, Supplement_2 (June 1, 2021): S11—S12. http://dx.doi.org/10.1093/jpids/piab031.025.

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Abstract Background The molecular mechanisms underpinning the neurologic and congenital pathologies caused by Zika virus (ZIKV) infection remain poorly understood. It is also unclear why congenital ZIKV disease was not reported prior to the recent epidemics in French Polynesia and the Americas, despite evidence that Zika virus has actively circulated in parts of Africa and Asia since 1947 and 1966, respectively. Methods Due to advances in the stem cell-based technologies, we can now model ZIKV infections of the central nervous system in human stem cell-derived neural progenitor cells and cerebral organoids, which recapitulate complex 3-dimensional neural architecture. We apply Seq-Well — a simple, portable platform for massively parallel single-cell RNA sequencing — to characterize these neural models infected with ZIKV. We detect and quantify host mRNA transcripts and viral RNA with single-cell resolution, thereby defining transcriptional features of both uninfected and infected cells. Results Although flavivirus RNAs lack a poly(A) tail, we present evidence that viral RNAs are specifically primed for reverse transcription at internal runs of adenosines, and that sequencing reads cover the entire non-polyadenylated viral genome. In neural progenitor cells, single cell sequencing reveals that while uninfected bystander cells strongly upregulate interferon pathway genes, these pathways are largely suppressed in cells infected with ZIKV within the same culture dish. Single cell sequencing identifies multiple cell types in our cerebral organoids including neural progenitor cells, intermediate progenitor cells, and neurons of varied maturity. Using this model, we find that neurons, not typically considered targets of ZIKV in the developing brain, contain high copy numbers of ZIKV genomes. It remains uncertain whether neurons are directly infected, or if infected neural progenitor cells differentiate into neurons, carrying virus with them. Notably, the neuronal bystander cell population shows limited interferon gene pathway upregulation compared to neural progenitors. Conclusions Overall, our work provides insight into the pathogenesis of ZIKV associated microcephaly, identifies potential new tropisms of ZIKV in the human brain, and suggests that both virus replication and host response mechanisms underlie the neuropathology of ZIKV infection.
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Ojalvo-Sanz, Ana Cristina, and Laura López-Mascaraque. "Gliogenic Potential of Single Pallial Radial Glial Cells in Lower Cortical Layers." Cells 10, no. 11 (November 19, 2021): 3237. http://dx.doi.org/10.3390/cells10113237.

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During embryonic development, progenitor cells are progressively restricted in their potential to generate different neural cells. A specific progenitor cell type, the radial glial cells, divides symmetrically and then asymmetrically to produce neurons, astrocytes, oligodendrocytes, and NG2-glia in the cerebral cortex. However, the potential of individual progenitors to form glial lineages remains poorly understood. To further investigate the cell progeny of single pallial GFAP-expressing progenitors, we used the in vivo genetic lineage-tracing method, the UbC-(GFAP-PB)-StarTrack. After targeting those progenitors in embryonic mice brains, we tracked their adult glial progeny in lower cortical layers. Clonal analyses revealed the presence of clones containing sibling cells of either a glial cell type (uniform clones) or two different glial cell types (mixed clones). Further, the clonal size and rostro-caudal cell dispersion of sibling cells differed depending on the cell type. We concluded that pallial E14 neural progenitors are a heterogeneous cell population with respect to which glial cell type they produce, as well as the clonal size of their cell progeny.
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Neckel, Peter Helmut, Roland Mohr, Ying Zhang, Bernhard Hirt, and Lothar Just. "Comparative Microarray Analysis of Proliferating and Differentiating Murine ENS Progenitor Cells." Stem Cells International 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/9695827.

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Postnatal neural progenitor cells of the enteric nervous system are a potential source for future cell replacement therapies of developmental dysplasia like Hirschsprung’s disease. However, little is known about the molecular mechanisms driving the homeostasis and differentiation of this cell pool. In this work, we conducted Affymetrix GeneChip experiments to identify differences in gene regulation between proliferation and early differentiation of enteric neural progenitors from neonatal mice. We detected a total of 1333 regulated genes that were linked to different groups of cellular mechanisms involved in cell cycle, apoptosis, neural proliferation, and differentiation. As expected, we found an augmented inhibition in the gene expression of cell cycle progression as well as an enhanced mRNA expression of neuronal and glial differentiation markers. We further found a marked inactivation of the canonical Wnt pathway after the induction of cellular differentiation. Taken together, these data demonstrate the various molecular mechanisms taking place during the proliferation and early differentiation of enteric neural progenitor cells.
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McClellan, Kelly A., Jacqueline L. Vanderluit, Lisa M. Julian, Matthew G. Andrusiak, Delphie Dugal-Tessier, David S. Park, and Ruth S. Slack. "The p107/E2F Pathway Regulates Fibroblast Growth Factor 2 Responsiveness in Neural Precursor Cells." Molecular and Cellular Biology 29, no. 17 (June 29, 2009): 4701–13. http://dx.doi.org/10.1128/mcb.01767-08.

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ABSTRACT We have previously shown that p107, a member of the retinoblastoma (Rb) cell cycle regulatory family, has a unique function in regulating the pool of neural precursor cells. As the pool of progenitors is regulated by a limiting supply of trophic factors, we asked if the Rb/E2F pathway may control the size of the progenitor population by regulating the levels of growth factors or their receptors. Here, we demonstrate that fibroblast growth factor 2 (FGF2) is aberrantly upregulated in the brains of animals lacking Rb family proteins and that the gene encoding the FGF2 ligand is directly regulated by p107 and E2F3. Chromatin immunoprecipitation assays demonstrated that E2F3 and p107 occupy E2F consensus sites on the FGF2 promoter in the context of native chromatin. To evaluate the physiological consequence of FGF2 deregulation in both p107 and E2F3 mutants, we measured neural progenitor responsiveness to growth factors. Our results demonstrate that E2F3 and p107 are each mediators of FGF2 growth factor responsiveness in neural progenitor cells. These results support a model whereby p107 regulates the pool of FGF-responsive progenitors by directly regulating FGF2 gene expression in vivo. By identifying novel roles for p107/E2F in regulating genes outside of the classical cell cycle machinery targets, we uncover a new mechanism whereby Rb/E2F mediates proliferation through regulating growth factor responsiveness.
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Qiu, Runxiang, Xiuyun Wang, Alice Davy, Chen Wu, Kiyohito Murai, Heying Zhang, John G. Flanagan, Philippe Soriano, and Qiang Lu. "Regulation of neural progenitor cell state by ephrin-B." Journal of Cell Biology 181, no. 6 (June 9, 2008): 973–83. http://dx.doi.org/10.1083/jcb.200708091.

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Maintaining a balance between self-renewal and differentiation in neural progenitor cells during development is important to ensure that correct numbers of neural cells are generated. We report that the ephrin-B–PDZ-RGS3 signaling pathway functions to regulate this balance in the developing mammalian cerebral cortex. During cortical neurogenesis, expression of ephrin-B1 and PDZ-RGS3 is specifically seen in progenitor cells and is turned off at the onset of neuronal differentiation. Persistent expression of ephrin-B1 and PDZ-RGS3 prevents differentiation of neural progenitor cells. Blocking RGS-mediated ephrin-B1 signaling in progenitor cells through RNA interference or expression of dominant-negative mutants results in differentiation. Genetic knockout of ephrin-B1 causes early cell cycle exit and leads to a concomitant loss of neural progenitor cells. Our results indicate that ephrin-B function is critical for the maintenance of the neural progenitor cell state and that this role of ephrin-B is mediated by PDZ-RGS3, likely via interacting with the noncanonical G protein signaling pathway, which is essential in neural progenitor asymmetrical cell division.
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Noisa, Parinya, Taneli Raivio, and Wei Cui. "Neural Progenitor Cells Derived from Human Embryonic Stem Cells as an Origin of Dopaminergic Neurons." Stem Cells International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/647437.

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Human embryonic stem cells (hESCs) are able to proliferatein vitroindefinitely without losing their ability to differentiate into multiple cell types upon exposure to appropriate signals. Particularly, the ability of hESCs to differentiate into neuronal subtypes is fundamental to develop cell-based therapies for several neurodegenerative disorders, such as Alzheimer’s disease, Huntington’s disease, and Parkinson’s disease. In this study, we differentiated hESCs to dopaminergic neurons via an intermediate stage, neural progenitor cells (NPCs). hESCs were induced to neural progenitor cells by Dorsomorphin, a small molecule that inhibits BMP signalling. The resulting neural progenitor cells exhibited neural bipolarity with high expression of neural progenitor genes and possessed multipotential differentiation ability. CBF1 and bFGF responsiveness of these hES-NP cells suggested their similarity to embryonic neural progenitor cells. A substantial number of dopaminergic neurons were derived from hES-NP cells upon supplementation of FGF8 and SHH, key dopaminergic neuron inducers. Importantly, multiple markers of midbrain neurons were detected, includingNURR1, PITX3, andEN1, suggesting that hESC-derived dopaminergic neurons attained the midbrain identity. Altogether, this work underscored the generation of neural progenitor cells that retain the properties of embryonic neural progenitor cells. These cells will serve as an unlimited source for the derivation of dopaminergic neurons, which might be applicable for treating patients with Parkinson’s disease.
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Azemi, Erdrin, Glenn T. Gobbel, and Xinyan Tracy Cui. "Seeding neural progenitor cells on silicon-based neural probes." Journal of Neurosurgery 113, no. 3 (September 2010): 673–81. http://dx.doi.org/10.3171/2010.1.jns09313.

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Object Chronically implanted neural electrode arrays have the potential to be used as neural prostheses in patients with various neurological disorders. While these electrodes perform well in acute recordings, they often fail to function reliably in clinically relevant chronic settings because of glial encapsulation and the loss of neurons. Surface modification of these implants may provide a means of improving their biocompatibility and integration within host brain tissue. The authors proposed a method of improving the brain-implant interface by seeding the implant's surface with a layer of neural progenitor cells (NPCs) derived from adult murine subependyma. Neural progenitor cells may reduce the foreign body reaction by presenting a tissue-friendly surface and repair implant-induced injury and inflammation by releasing neurotrophic factors. In this study, the authors evaluated the growth and differentiation of NPCs on laminin-immobilized probe surfaces and explored the potential impact on transplant survival of these cells. Methods Laminin protein was successfully immobilized on the silicon surface via covalent binding using silane chemistry. The growth, adhesion, and differentiation of NPCs expressing green fluorescent protein (GFP) on laminin-modified silicon surfaces were characterized in vitro by using immunocytochemical techniques. Shear forces were applied to NPC cultures in growth medium to evaluate their shearing properties. In addition, neural probes seeded with GFP-labeled NPCs cultured in growth medium for 14 days were implanted in murine cortex. The authors assessed the adhesion properties of these cells during implantation conditions. Moreover, the tissue response around NPC-seeded implants was observed after 1 and 7 days postimplantation. Results Significantly improved NPC attachment and growth was found on the laminin-immobilized surface compared with an unmodified control before and after shear force application. The NPCs grown on the laminin-immobilized surface showed differentiation potential similar to those grown on polylysine-treated well plates, as previously reported. Viable (still expressing GFP) NPCs were found on and in proximity to the neural implant after 1 and 7 days postimplantation. Preliminary examinations indicated that the probe's NPC coating might reduce the glial response at these 2 different time points. Conclusions The authors' findings suggest that NPCs can differentiate and strongly adhere to laminin-immobilized surfaces, providing a stable matrix for these cells to be implanted in brain tissue on the neural probe's surface. In addition, NPCs were found to improve the astrocytic reaction around the implant site. Further in vivo work revealing the mechanisms of this effect could lead to improvement of biocompatibility and chronic recording performance of neural probes.
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Chalasani, Kavita, and Rachel M. Brewster. "N-cadherin–mediated cell adhesion restricts cell proliferation in the dorsal neural tube." Molecular Biology of the Cell 22, no. 9 (May 2011): 1505–15. http://dx.doi.org/10.1091/mbc.e10-08-0675.

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Neural progenitors are organized as a pseudostratified epithelium held together by adherens junctions (AJs), multiprotein complexes composed of cadherins and α- and β-catenin. Catenins are known to control neural progenitor division; however, it is not known whether they function in this capacity as cadherin binding partners, as there is little evidence that cadherins themselves regulate neural proliferation. We show here that zebrafish N-cadherin (N-cad) restricts cell proliferation in the dorsal region of the neural tube by regulating cell-cycle length. We further reveal that N-cad couples cell-cycle exit and differentiation, as a fraction of neurons are mitotic in N-cad mutants. Enhanced proliferation in N-cad mutants is mediated by ligand-independent activation of Hedgehog (Hh) signaling, possibly caused by defective ciliogenesis. Furthermore, depletion of Hh signaling results in the loss of junctional markers. We therefore propose that N-cad restricts the response of dorsal neural progenitors to Hh and that Hh signaling limits the range of its own activity by promoting AJ assembly. Taken together, these observations emphasize a key role for N-cad–mediated adhesion in controlling neural progenitor proliferation. In addition, these findings are the first to demonstrate a requirement for cadherins in synchronizing cell-cycle exit and differentiation and a reciprocal interaction between AJs and Hh signaling.
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Reid, K., A. M. Turnley, G. D. Maxwell, Y. Kurihara, H. Kurihara, P. F. Bartlett, and M. Murphy. "Multiple roles for endothelin in melanocyte development: regulation of progenitor number and stimulation of differentiation." Development 122, no. 12 (December 1, 1996): 3911–19. http://dx.doi.org/10.1242/dev.122.12.3911.

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Melanocytes in the skin are derived from the embryonic neural crest. Recently, mutations in endothelin 3 and the endothelin receptor B genes have been shown to result in gross pigment defects, indicating that this signalling pathway is required for melanocyte development. We have examined the effects of endothelins on melanocyte progenitors in cultures of mouse neural crest. Firstly, they stimulate an increase in progenitor number and act synergistically with another factor, Steel factor, in the survival and proliferation of the progenitors. These findings are consistent with findings from mice with natural mutations in the endothelin receptor B gene, which show an early loss of melanocyte progenitors. Secondly, endothelins induce differentiation of the progenitors into fully mature pigmented melanocytes. This finding is consistent with the expression of endothelins in the skin of mice at the initiation of pigmentation. The melanocytes generated in endothelin-treated cultures also become responsive to alpha melanocyte-stimulating hormone, which then acts to regulate the activity of the pigmentation pathway. These findings indicate two key roles for endothelin in melanocyte development: regulation of expansion of the progenitor pool and differentiation of progenitors into mature melanocytes.
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Crane, Jennifer F., and Paul A. Trainor. "Neural Crest Stem and Progenitor Cells." Annual Review of Cell and Developmental Biology 22, no. 1 (November 2006): 267–86. http://dx.doi.org/10.1146/annurev.cellbio.22.010305.103814.

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Drapeau, Pierre. "Neurotransmitter regulation of neural progenitor differentiation." Neuroscience Research 71 (September 2011): e37. http://dx.doi.org/10.1016/j.neures.2011.07.163.

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Pevny, Larysa, and Marysia Placzek. "SOX genes and neural progenitor identity." Current Opinion in Neurobiology 15, no. 1 (February 2005): 7–13. http://dx.doi.org/10.1016/j.conb.2005.01.016.

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Liu, Helio C., Grigori Enikolopov, and Yuzhi Chen. "Cul4B regulates neural progenitor cell growth." BMC Neuroscience 13, no. 1 (2012): 112. http://dx.doi.org/10.1186/1471-2202-13-112.

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Mehler, Mark F., and John A. Kessler. "Neural progenitor cells and developmental disorders." Mental Retardation and Developmental Disabilities Research Reviews 4, no. 3 (1998): 143–49. http://dx.doi.org/10.1002/(sici)1098-2779(1998)4:3<143::aid-mrdd1>3.0.co;2-p.

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Gao, Mingyong, Haiyin Tao, Tao Wang, Ailin Wei, and Bin He. "Functionalized self-assembly polypeptide hydrogel scaffold applied in modulation of neural progenitor cell behavior." Journal of Bioactive and Compatible Polymers 32, no. 1 (September 21, 2016): 45–60. http://dx.doi.org/10.1177/0883911516653146.

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Three-dimensional cell culturing provides an appealing biomimetic platform to probe the biological effects of a designed extracellular matrix on the behavior of seeded neural stem or neural progenitor cells. This culturing model serves as an important tool to investigate functional regulators involved in proliferation and differentiation of neural progenitor cells. This study aims to reconstruct a polypeptide hydrogel matrix functionally integrated with cyclo-RGD motif [c(RGDfK)] for initial exploration of neural progenitor cell behavior in three-dimensional culture. Three types of hydrogel scaffolds including Type I collagen, RADA16 self-assembly peptide, and RADA16-c(RGDfK) self-assembly peptide hydrogel were employed to serve as the culturing extracellular matrix of neonatal rat spinal neural progenitor cells. The neural adhesion of functionalized self-assembly peptide hydrogel was acquired prior to its RADA16 counterpart with neural progenitor cell seeding tests. The biophysiological properties of self-assembly peptide hydrogel scaffolds were then detected by scanning electron microscopy and rheology measurements. The biological behavior of embedded neural progenitor cells including cell proliferation and differentiation in three-dimensional niche were analyzed by MTT [(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide)] tests and immunocytochemistry fluorescence staining. The 1% (w/v) RADA16-c(RGDfK) hydrogel scaffold [R16-c(RGDfK)HS] demonstrated an elastic modulus(312 ± 5.7 Pa) compatible with central neural cells, which significantly facilitated the proliferation of embedded neural progenitor cells. Compared to collagen hydrogel, both RADA16 and RADA16-c(RGDfK) hydrogel scaffold improved the cellular proliferation and neuronal differentiation of neural progenitor cells in a three-dimensional culture model. In order to model neuronal regeneration, introduction of neurotrophin-3 in the differentiation environment significantly increased the neuronal differentiation in which the ratio of Tuj-1-positive cell number increased to 72.5% ± 4.7% in the c(RGDfK)-functionalized three-dimensional matrix environment at 7 days in culture. Collectively, the present R16-c(RGDfK)HS displays excellent central neural biocompatibility and emerges as a promising bioengineered extracellular matrix niche of neural stem or progenitor cells, building a solid foundation for the subsequent in vitro and in vivo studies including neural repair, regeneration, and development.
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Olmos-Carreño, Cindy L., María Figueres-Oñate, Gabriel E. Scicolone, and Laura López-Mascaraque. "Cell Fate of Retinal Progenitor Cells: In Ovo UbC-StarTrack Analysis." International Journal of Molecular Sciences 23, no. 20 (October 16, 2022): 12388. http://dx.doi.org/10.3390/ijms232012388.

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Clonal cell analysis outlines the ontogenic potential of single progenitor cells, allowing the elucidation of the neural heterogeneity among different cell types and their lineages. In this work, we analyze the potency of retinal stem/progenitor cells through development using the chick embryo as a model. We implemented in ovo the clonal genetic tracing strategy UbC-StarTrack for tracking retinal cell lineages derived from individual progenitors of the ciliary margin at E3.5 (HH21-22). The clonal assignment of the derived-cell progeny was performed in the neural retina at E11.5-12 (HH38) through the identification of sibling cells as cells expressing the same combination of fluorophores. Moreover, cell types were assessed based on their cellular morphology and laminar location. Ciliary margin derived-cell progenies are organized in columnar associations distributed along the peripheral retina with a limited tangential dispersion. The analysis revealed that, at the early stages of development, this region harbors multipotent and committed progenitor cells.
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Yin, Chonghai, Xin Zhou, Yong-Gang Yao, Wei Wang, Qian Wu, and Xiaoqun Wang. "Abundant Self-Amplifying Intermediate Progenitors in the Subventricular Zone of the Chinese Tree Shrew Neocortex." Cerebral Cortex 30, no. 5 (February 20, 2020): 3370–80. http://dx.doi.org/10.1093/cercor/bhz315.

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Abstract During evolution, neural progenitor cells in the subventricular zone (SVZ) have fundamental functions, ranging from brain volume expansion to the generation of a six-layered neocortex. In lissencephalic animal models, such as rodents, the majority of neural progenitors in the SVZ are intermediate progenitor cells (IPCs). Most IPCs in rodents undergo neurogenic division, and only a small portion of them divide a very limited number of times to generate a few neurons. Meanwhile, in gyrencephalic animals, such as primates, IPCs are able to self-renew for up to five successive divisions. However, abundant IPCs with successive proliferative capacity have not been directly observed in nonprimate species. In this study, we examined the development of neural progenitors in the Chinese tree shrew (Tupaia belangeri chinensis), a lissencephalic animal with closer affinity than rodents to primates. We identified an expansion of the SVZ and the presence of outer radial glial (oRG) cells in the neocortex. We also found that IPCs have the capacity to self-amplify multiple times and therefore serve as major proliferative progenitors. To our knowledge, our study provides the first direct evidence of abundant IPCs with proliferative potential in a nonprimate species, further supporting the key role of IPCs in brain expansion.
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Zhang, Huanxiang, Laszlo Vutskits, Michael S. Pepper, and Jozsef Z. Kiss. "VEGF is a chemoattractant for FGF-2–stimulated neural progenitors." Journal of Cell Biology 163, no. 6 (December 22, 2003): 1375–84. http://dx.doi.org/10.1083/jcb.200308040.

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Mmigration of undifferentiated neural progenitors is critical for the development and repair of the nervous system. However, the mechanisms and factors that regulate migration are not well understood. Here, we show that vascular endothelial growth factor (VEGF)-A, a major angiogenic factor, guides the directed migration of neural progenitors that do not display antigenic markers for neuron- or glia-restricted precursor cells. We demonstrate that progenitor cells express both VEGF receptor (VEGFR) 1 and VEGFR2, but signaling through VEGFR2 specifically mediates the chemotactic effect of VEGF. The expression of VEGFRs and the chemotaxis of progenitors in response to VEGF require the presence of fibroblast growth factor 2. These results demonstrate that VEGF is an attractive guidance cue for the migration of undifferentiated neural progenitors and offer a mechanistic link between neurogenesis and angiogenesis in the nervous system.
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Lian, Gewei, Timothy Wong, Jie Lu, Jianjun Hu, Jingping Zhang, and Volney Sheen. "Cytoskeletal Associated Filamin A and RhoA Affect Neural Progenitor Specification During Mitosis." Cerebral Cortex 29, no. 3 (February 16, 2018): 1280–90. http://dx.doi.org/10.1093/cercor/bhy033.

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Abstract Neural progenitor proliferation and cell fate decision from self-renewal to differentiation are crucial factors in determining brain size and morphology. The cytoskeletal dependent regulation of these processes is not entirely known. The actin-binding filamin A (FlnA) was shown to regulate proliferation of progenitors by directing changes in cell cycles proteins such as Cdk1 during G2/M phase. Here we report that functional loss of FlnA not only affects the rate of proliferation by altering cell cycle length but also causes a defect in early differentiation through changes in cell fate specification. FlnA interacts with Rho GTPase RhoA, and FlnA loss impairs RhoA activation. Disruption of either of these cytoskeletal associated proteins delays neurogenesis and promotes neural progenitors to remain in proliferative states. Aurora kinase B (Aurkb) has been implicated in cytokinesis, and peaks in expression during the G2/M phase. Inhibition of FlnA or RhoA impairs Aurkb degradation and alters its localization during mitosis. Overexpression of Aurkb replicates the same delay in neurogenesis seen with loss of FlnA or RhoA. Our findings suggest that shared cytoskeletal processes can direct neural progenitor proliferation by regulating the expression and localization of proteins that are implicated in the cell cycle progression and cell fate specification.
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Turrero García, Miguel, José-Manuel Baizabal, Diana N. Tran, Rui Peixoto, Wengang Wang, Yajun Xie, Manal A. Adam, et al. "Transcriptional regulation of MGE progenitor proliferation by PRDM16 controls cortical GABAergic interneuron production." Development 147, no. 22 (October 15, 2020): dev187526. http://dx.doi.org/10.1242/dev.187526.

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ABSTRACTThe mammalian cortex is populated by neurons derived from neural progenitors located throughout the embryonic telencephalon. Excitatory neurons are derived from the dorsal telencephalon, whereas inhibitory interneurons are generated in its ventral portion. The transcriptional regulator PRDM16 is expressed by radial glia, neural progenitors present in both regions; however, its mechanisms of action are still not fully understood. It is unclear whether PRDM16 plays a similar role in neurogenesis in both dorsal and ventral progenitor lineages and, if so, whether it regulates common or unique networks of genes. Here, we show that Prdm16 expression in mouse medial ganglionic eminence (MGE) progenitors is required for maintaining their proliferative capacity and for the production of proper numbers of forebrain GABAergic interneurons. PRDM16 binds to cis-regulatory elements and represses the expression of region-specific neuronal differentiation genes, thereby controlling the timing of neuronal maturation. PRDM16 regulates convergent developmental gene expression programs in the cortex and MGE, which utilize both common and region-specific sets of genes to control the proliferative capacity of neural progenitors, ensuring the generation of correct numbers of cortical neurons.
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Wang, Yafei, Zhiheng Lu, Yilan Zhang, Yuqun Cai, Di Yun, Tianxiang Tang, Zheping Cai, et al. "Transcription Factor 4 Safeguards Hippocampal Dentate Gyrus Development by Regulating Neural Progenitor Migration." Cerebral Cortex 30, no. 5 (December 14, 2019): 3102–15. http://dx.doi.org/10.1093/cercor/bhz297.

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Abstract The dentate gyrus (DG) of the hippocampal formation plays essential roles in learning and memory. Defective DG development is associated with neurological disorders. Here, we show that transcription factor 4 (Tcf4) is essential for DG development. Tcf4 expression is elevated in neural progenitors of the dentate neuroepithelium in the developing mouse brain. We demonstrate that conditional disruption of Tcf4 in the dentate neuroepithelium leads to abnormal neural progenitor migration guided by disorganized radial glial fibers, which further leads to hypoplasia in the DG. Moreover, we reveal that Wnt7b is a key downstream effector of Tcf4 in regulating neural progenitor migration. Behavioral analysis shows that disruption of integrity of the DG impairs the social memory highlighting the importance of proper development of the DG. These results reveal a critical role for Tcf4 in regulating DG development. As mutations in TCF4 cause Pitt–Hopkins syndrome (PTHS) characterized by severe intellectual disability, our data also potentially provide insights into the basis of neurological defects linked to TCF4 mutations.
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Moore, Rachel, and Paula Alexandre. "Delta-Notch Signaling: The Long and The Short of a Neuron’s Influence on Progenitor Fates." Journal of Developmental Biology 8, no. 2 (March 26, 2020): 8. http://dx.doi.org/10.3390/jdb8020008.

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Maintenance of the neural progenitor pool during embryonic development is essential to promote growth of the central nervous system (CNS). The CNS is initially formed by tightly compacted proliferative neuroepithelial cells that later acquire radial glial characteristics and continue to divide at the ventricular (apical) and pial (basal) surface of the neuroepithelium to generate neurons. While neural progenitors such as neuroepithelial cells and apical radial glia form strong connections with their neighbours at the apical and basal surfaces of the neuroepithelium, neurons usually form the mantle layer at the basal surface. This review will discuss the existing evidence that supports a role for neurons, from early stages of differentiation, in promoting progenitor cell fates in the vertebrates CNS, maintaining tissue homeostasis and regulating spatiotemporal patterning of neuronal differentiation through Delta-Notch signalling.
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Stephens, Crystal L., Hiroki Toda, Theo D. Palmer, Thomas B. DeMarse, and Brandi K. Ormerod. "Adult neural progenitor cells reactivate superbursting in mature neural networks." Experimental Neurology 234, no. 1 (March 2012): 20–30. http://dx.doi.org/10.1016/j.expneurol.2011.12.009.

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Reichert, Karine P., Maria Rosa C. Schetinger, Micheli M. Pillat, Nathieli B. Bottari, Tais V. Palma, Jessie M. Gutierres, Henning Ulrich, Cinthia M. Andrade, Christopher Exley, and Vera M. M. Morsch. "Aluminum affects neural phenotype determination of embryonic neural progenitor cells." Archives of Toxicology 93, no. 9 (July 30, 2019): 2515–24. http://dx.doi.org/10.1007/s00204-019-02522-6.

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Donega, Vanessa, and Olivier Raineteau. "Postnatal Neural Stem Cells: Probing Their Competence for Cortical Repair." Neuroscientist 23, no. 6 (March 16, 2017): 605–15. http://dx.doi.org/10.1177/1073858417697036.

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There is growing evidence for a tentative cellular repair in the forebrain following perinatal injuries. In this review, we present the evidences and shortcomings in this regenerative attempt. We discuss recent progress in elucidating the origin, diversity, and competence of postnatal neural stem cells/progenitor cells. Finally, we propose new strategies to recruit postnatal progenitors to generate specific subtypes of cortical neurons or oligodendrocytes, thereby allowing the development of tailor-made approaches to treat perinatal brain injuries.
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